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Physicians who use electroconvulsivetherapy (ECT) need tobe vigilant for unstable medicalconditions before and during the courseof treatment. This brief review is intendedto highlight some basic principlesand specific concerns that maybe encountered in the use of ECT inpatients who have comorbid medicalillness.
April 2006, Vol. XXIII, No. 5
Physicians who use electroconvulsivetherapy (ECT) need tobe vigilant for unstable medicalconditions before and during the courseof treatment. This brief review is intendedto highlight some basic principlesand specific concerns that maybe encountered in the use of ECT inpatients who have comorbid medicalillness. For more extensive discussions,I refer the reader to recent reviews ofECT in the medically ill by Abrams1and Rasmussen and colleagues,2 aswell as the recommendations of theAmerican Psychiatric AssociationCommittee on ECT.3
Safe use of ECT in the medically illpatient begins with a careful pretreatmentevaluation. The cornerstones ofthis are the medical history, review ofsystems, and physical examination,which together are far more important than blood tests or other diagnostic studies.Any significant abnormalities thatemerge, especially those relevant to thecardiac, respiratory, or neurologic systems,can be investigated with a rationalchoice of diagnostic tests and medicalconsultations. For example, in patientswith unstable heart disease, an echocardiogrammay be helpful in assessinghow the heart will react to the stress ofan ECT treatment and may indicate theneed for pretreatment modification ofthe patient's medication regimen.
Routine pre-ECT tests should includeserum electrolyte levels and anECG. A chest xray study should beconsidered in elderly patients and inthose with pulmonary disorders. Brainimaging studies, such as CT or MRI,are not routinely needed but should beconsidered for those in whom thehistory or physical examination suggestsstructural CNS pathology.
The second principle is careful monitoringof the patient during each treatment.If cardiac medications, glaucomaeyedrops, or inhalers are prescribed,these should be administered beforeeach treatment.2,3 For patients withsevere cardiac disease, tight control of blood pressure may be advisable;accordingly, antihypertensive medicationscan be used in the treatment suite.
The third basic principle for themedically ill patient receiving ECT is(CHF) who was well compensatedcardiologically before the first treatmentmay be having some pulmonary congestionafter several treatments. Onlyongoing evaluation of the medical statusthroughout treatment to monitor fordestabilization of existing conditions oremergence of new ones. For example,a patient with congestive heart failure through daily history taking and physicalexamination can the physician detectsuch subtle changes.
Abrams1 and Rasmussen and colleagues2provide detailed discussions about themedical physiology of ECT seizures, anunderstanding of which helps informmanagement before and during ECT inpatients with medical conditions. I willreview this topic only briefly here. Themain organ systems affected duringseizures are the brain, of course, and theheart. Over the decades, there has beena plethora of research on neurometaboliceffects of electrically induced seizuresin humans and animals, none of whichspecifically has implications at presentfor ECT in medically ill patients.
From a neurovascular standpoint, arapid increase in cerebral perfusionoccurs, resulting in increased permeabilityof the blood-brain barrier as wellas a temporary rise in intracranial pressure.Such changes would be expectedto have implications for patients withspace-occupying lesions and increasedintracranial pressure (eg, brain tumors).Another robust neurophysiologicchange in ECT is a rise in the electricallyinduced seizure threshold (thus,an anticonvulsant effect), an interestingphenomenon that has formed thebasis for the occasional use of ECT toreduce spontaneous seizure frequencyin patients with epilepsy.4
The cardiac physiologic effects ofECT have been well characterized.Barbiturate anesthetics have a slightdepressing effect on blood pressure.Immediately after the presentation ofthe electrical stimulus, there is a sometimesprofound parasympathetic stimulationthat leads to a few seconds ofasystole.5 This is rapidly replaced by asympathetic predominance (assumingthat the electrical stimulus was of sufficientintensity to produce a seizure)that leads to a sharp rise in heart rateand blood pressure, effects that abateshortly after the end of the seizure. Inaddition, various arrhythmias, such aspremature ventricular contractions, prematureatrial contractions, and evenvery brief runs of ventricular tachycardiawithout blood pressure compromise,are quite common. These variousphysiologic changes would clearly haveimplications for patients with cardiacconditions such as congestive heart failure,coronary artery disease, cardiomyopathies,and arrhythmias.
Given the physiologic changes associatedwith ECT, it bears repeating thata thorough pre-ECT evaluation, carefulmanagement during treatments, andvigilant intertreatment monitoring formthe bulwark of care for patients withany medical illness who undergo ECT.
The most common cardiac conditionsencountered in ECT practice are coronaryartery disease, CHF, and arrhythmias.For the patient with coronaryartery disease, the internist or cardiologistwill want to ask detailed questionsabout exercise tolerance, angina pectoris,and shortness of breath. Cardiac auscultationwill also provide informationabout the stability of myocardial function.Consultation with a cardiologist orwith an internist familiar with ECT issuggested for such patients. Pretreatmentdiagnostic tests, such as echocardiographyor nuclear medicine scanning,may assess how the patient's heart respondsto the increased myocardial workloadthat occurs during seizures.
If evidence of ventricular wall motionabnormalities or ischemic changes ispresent, then cardiac medication changesor even revascularization proceduresshould be considered before ECT. If thecardiologist does not recommend sucha course of action, then considerationmay be given to use of β-blockers duringthe ECT treatments to lessen the increasein myocardial workload. Communicationbetween the attending cardiologistand anesthesiologist is crucial tosettle on a rational management plan.
CHF presents a special challenge in ECT, because patients with CHF are oftenexquisitely sensitive to increases in myocardialoxygen demand.2 Again, cardiologicconsultation is recommended forsuch patients to optimize their medicationregimen before ECT is begun; a marginallycompensated patient may easilyproceed to frank decompensation aftera few treatments.6 It is important to administerthe patient's prescribed cardiacmedication regimen, including diuretics,on the morning of each ECT treatment.
The most common arrhythmia inpatients receiving ECT is atrial fibrillation.There are numerous reports ofsafe use of ECT in patients with atrialfibrillation, but conversion to normalsinus rhythm has been described andthe risk of thrombus/embolus formationis also present.7 Thus, maintaininganticoagulation with warfarin or heparinduring ECT is usually recommended insuch patients. If the heart rate is notcontrolled at baseline, the cardiologistwill probably recommend treatment tocontrol it before proceeding with ECT.Patients with pacemakers or implantablecardioverter-defibrillators (ICDs) can betreated safely with ECT; recommendedmanagement includes pretreatmentdevice interrogation to ensure properfunction and turning off of ICDs (aftercontinuous ECG monitoring has beenstarted) under the guidance of competentpersonnel.8
The most common neurologic illnessin patients receiving ECT is dementia,usually of the Alzheimer or Lewy bodytype. Numerous case series have documentedthat demented patients can attainsignificant benefit in mood and disruptivebehaviors with ECT without apparentlong-term worsening of thedementing process.9 I recommend thatdemented patients be treated with unilateralor bifrontal electrode placement tolessen cognitive effects. Patients whohave Parkinson disease (PD) often experiencemotoric improvement with ECT,possibly as a result of enhanced dopaminergicfunction.10
On the other hand, some evidencesuggests that in patients with basalganglia dysfunction, such as those withPD, ECT may have excessive cognitiveeffects, so either unilateral or bifrontalelectrode placement is recommendedin these patients. There may also bedyskinesias during ECT in patients withPD who are taking levodopa, so thedosage of that drug may need to bereduced temporarily during the courseof treatments.10
Because of the increase in intracranialpressure during seizures, braintumors or other intracranial masses--especially those associated with increasedintracranial pressure--may posea substantial risk of neurologic deterioration deteriorationduring ECT.11 Several case reportsdo seem to indicate that meningiomasnot associated with edema or mass effectmay pose no increased risk during ECT.12
There is no evidence that ECT worsensthe course of epilepsy; in fact, it mayreduce the frequency of spontaneousseizures in patients with epilepsy.4 However,seizure induction may be difficultif the patient is taking anticonvulsant medication.Cautious dose reduction of suchmedications, if deemed safe by thepatient's neurologist, may result in enhancedseizure expression during ECT.
Patients with neuroleptic malignantsyndrome (or other forms of malignantcatatonia) may experience dramaticimprovement with ECT.3 Patients witha wide variety of other neurologic conditions,as documented in an extensive casereport literature, can be treated safelywith ECT.2 A possible exception is multiplesclerosis, especially with gadoliniumenhancinglesions on MRI; there is onereport of neurologic worsening withECT in a patient with such lesions.13
If inhalers have been prescribed for apatient with chronic obstructive pulmonarydisease or asthma, these shouldbe administered before each treatment.Theophylline in patients receiving ECThas been associated with status epilepticus,and if the patient is taking this medication, blood levels should bechecked regularly.14
Patients with diabetes who are takinginsulin can be given half their usualmorning dose and treated promptlywith ECT, then given the remaining halfand fed breakfast. Non-insulin-dependentpersons should not be given theirmorning oral hypoglycemic agent untilafter the treatment, when they can eata meal. Blood sugar should be checkedbefore each treatment by fingerstick.
In the third trimester of pregnancy,the sympathetic stimulation associatedwith the seizure may be associated withabruptio placentae or premature labor.In such cases, noninvasive fetal monitoringis recommended; ECT shouldonly be conducted if obstetric servicesare readily available.3
Dr Rasmussen is associate professor, departmentof psychiatry, Mayo Clinic, Rochester,Minn. He reports no financial conflicts regardingthe subject matter of this article.
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11. Maltbie AA, Wingfield MS, Volow MR, et al.Electroconvulsive therapy in the presence of braintumor: case reports and an evaluation of risk. J NervMent Dis. 1980;168:400-405.
12. McKinney PA, Beale MD, Kellner CH.Electroconvulsive therapy in a patient with a cerebellarmeningioma. J ECT. 1998;14:49-52.
13. Mattingly G, Baker K, Zorumski CG, et al. Multiplesclerosis and ECT: possible value of gadoliniumenhancedmagnetic resonance scans for identifyinghigh-risk patients. J Neuropsychiatry Clin Neurosci.1993;4:145-151.
14. Rasmussen KG, Zorumski CF. ECT in patients takingtheophylline. J Clin Psychiatry. 1993;54:427-431.